Pathophysiology

Some tumors can progress to acute myeloid leukemia . It is a part of the disorders myeloproliferative chronic myeloid leukemia who became therapy radical phase of chronic development first , and syndromes other disorders myeloproliferative (fibrosis pure , thrombocythemia basic , polycythemia polyglobuli) in rare cases , LAM necessarily often cancer acute myeloid leukemia in the absence of the lymphatic system. This is another part of the myeloid dysplasia , anemia, especially with the heat resistance excess blasts (RAEB) or chronic leukemia sometimes Vahidi (CMML).
 Pathophysiology
AML of myeloid progenitor cells that can develop either pluripotent or already engaged in the granulocyte line as studies of clonality and marrow cultures shown . The mechanism of leukemogenesis would be "multi -step" with successive mutations of genes such as oncogenes or tumor suppressor genes leading to a leukemic phenotype.
Molecular analysis of structural changes in many genes identified karyotype may be involved in leukemogenesis . Some of these genes are oncogenes ( such as RAS or MYC ) or anti -oncogenes (such as RB or P53 ) is also involved in solid tumors , they do not seem to play an important role in leukemogenesis . Other genes are in particular in a specific type of LA .